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Science 299 (5604): 251-254

Copyright © 2003 by the American Association for the Advancement of Science

KCNQ1 Gain-of-Function Mutation in Familial Atrial Fibrillation

Yi-Han Chen,1*dagger Shi-Jie Xu,23*dagger Saïd Bendahhou,4 Xiao-Liang Wang,5 Ying Wang,2 Wen-Yuan Xu,1 Hong-Wei Jin,5 Hao Sun,2 Xiao-Yan Su,1 Qi-Nan Zhuang,2 Yi-Qing Yang,1 Yue-Bin Li,2 Yi Liu,1 Hong-Ju Xu,1 Xiao-Fei Li,1 Ning Ma,1 Chun-Ping Mou,1 Zhu Chen,26 Jacques Barhanin,4 Wei Huang236

Atrial fibrillation (AF) is a common cardiac arrhythmia whose molecular etiology is poorly understood. We studied a family with hereditary persistent AF and identified the causative mutation (S140G) in the KCNQ1 (KvLQT1) gene on chromosome 11p15.5. The KCNQ1 gene encodes the pore-forming alpha  subunit of the cardiac IKs channel (KCNQ1/KCNE1), the KCNQ1/KCNE2 and the KCNQ1/KCNE3 potassium channels. Functional analysis of the S140G mutant revealed a gain-of-function effect on the KCNQ1/KCNE1 and the KCNQ1/KCNE2 currents, which contrasts with the dominant negative or loss-of-function effects of the KCNQ1 mutations previously identified in patients with long QT syndrome. Thus, the S140G mutation is likely to initiate and maintain AF by reducing action potential duration and effective refractory period in atrial myocytes.

1 Department of Cardiology, Tongji Hospital, and Institute of Medical Genetics, Tongji University, 399 Xin Cun Road, Shanghai 200065, People's Republic of China.
2 Chinese National Human Genome Center at Shanghai, 250 Bi Bo Road, Shanghai 201203, People's Republic of China.
3 Health Science Center, Institute for Biological Sciences-Chinese Academy of Sciences and Shanghai Second Medical University, Shanghai 200025, People's Republic of China.
4 Institut de Pharmacologie Moléculaire et Cellulaire, CNRS, 660 Route des lucioles, 06560 Sophia Antipolis, France.
5 Institute of Materia Media, Chinese Academy of Medical Sciences, 1 Xian Nong Tan Street, Beijing 100050, People's Republic of China.
6 State Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Rui Jin Hospital affiliated to Shanghai Second Medical University, Shanghai 200025, People's Republic of China.
*   These authors contributed equally to this work.

dagger    To whom correspondence should be addressed. E-mail: drchen{at}public7.sta.net.cn (Y.-H.C.); xusj{at}chgc.sh.cn (S.-J. X.)



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